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Farm 2 Flashcards

1
Q

What are the bacterial causes of salivation in ruminants?

A

Calf diphtheria (necrobacillosis), F. necrophorum, necrotic laryngitis
Actinobacillosis (Wooden tongue)
Actinomycosis (Lumpy jaw)

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2
Q

What are the traumatic causes of salivation in ruminants?

A

Choke
Drenching gun/bolus injuries/oral burns
Teeth
Vagal nerve damage

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3
Q

Which viral diseases affect the oral cavity of ruminants?

A 
FMD 
Rabies 
BVDV 
BHV-1 (infectious bovine rhinotracheitis) 
MCF (malignant catarrhal fever, ovine herpes virus-2) 
Bovine papular stomatitis (BPSV) 
Orf (parapox virus) 
Bluetongue
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4
Q

Describe the orf vaccine

A

Live attenuated vaccine
Scratch vaccine done behind the elbow
VMD product database (do not vaccinate close to lambing, vaccination will not protect lambs via colostrum)

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5
Q

What are the clinical signs of bluetongue in sheep?

A

Eye and nasal discharges which becomes thick and crusty
Drooling as a result of swelling and/or ulcerations in the mouth
Swelling of the neck and/or the face, especially around the eyes and the muzzle
Severe lameness affected sheep are reluctant to rise
Haemorrhages into or under the skin
Inflammation and pain at the coronary band
A “blue tongue” is rarely a clinical sign of infection

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6
Q

What are the clinical signs of bluetongue in cattl?

A 
Possibly no signs of illness 
Nasal discharge
Swelling of the neck and head, especially around the eyes and muzzle
Conjunctivitis
Lameness
Saliva drooling out of the mouth
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7
Q

What is the causative agent of ‘wooden tongue’?

A

Actinobacillus lignieresi, gram -ve, facultive anaerobe, oxidase +ve, urease +ve, commensal of the MM

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8
Q

What are the clinical signs of wooden tongue?

A

Painful, sometimes fever
Stomatitis, glossitis, fibrous tissue, cellulitis evolving in pyogranulomatous infection
Swollen tongue, often protrudes, hard to the touch, submandibular swelling, enlarged Lnn
Salivation and reluctant to eat
Can also affect skin, oesophageal groove, rumen wall etc
May lead to vagal nerve injury

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9
Q

What is the treatment of wooden tongue?

A

Antibiotics (daily IM >10days)
Sodium iodide (IV, repeate every 10 days) risk it may cause restlessness, tachycardia and staggering
NSAIDs
Prevention: isolate cases and review feeding

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10
Q

What is the causative agent of lumpy jaw?

A

Actinomyces bovis, gram +ve rods , anaerobic or fa, NON-spore forming, form fungus like branched networks

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11
Q

What are the clinical signs of lumpy jaw?

A 
Swelling 
Abscesses 
Fistulous tracts
Fibrosis 
Mucosal damage 
Painful 
Suppurative granulation of the mandible and maxilla 
Hard immobile lesions
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12
Q

How is lumpy jaw treated?

A

Antibiotics: procaine benzylpenicillin (daily IM >10 days)
Sodium iodide
NSAIDs
The bone deformation will remain after treatment.

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13
Q

What is the causative agent of calf diphtheria (necrotic stomatitis)?

A

Fusobacterium necrophorum

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14
Q

What is the aeitiology of calf diphtheria (necrotic stomatitis)?

A

Trauma to buccal mucosa, erupting teeth, contaminated buckets, rough feed

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15
Q

What are the clinical signs of necrotic stomatitis?

A 
Common in calves under 3 mo
Necrotic lesions in the pharynx and larynx 
Swollen cheeks 
Salivation 
Foul smelling breath 
Painful swallowing 
Cough 
Inspiratory dyspnea 
Laryngeal form with stertor more common in older calves 3-18 mo
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16
Q

How is calf diphtheria (necrotic stomatitis) treated?

A

Isolation
Antibiotics (procaine benzylpenicillin daily IM >5 days)
NSAIDs
TLC
Tracheostomy
Can affect groups so discuss control with the farmer

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17
Q

What are the causes of stomatitis?

A

Traumatic injuries e.g. drenching gun
Foreign bodies e.g. sticks and root vegetables
Caustic substances on farm

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18
Q

How is stomatitis treated?

A

Remove decaying food material
Broad spec antibiotics (amoxicillin 5 days
NSAIDs
Discuss management practices

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19
Q

What is the life cycle of fasciola hepatica?

A

Eggs pass out in faeces
Eggs hatch, miracidians penetrate snail (Galba truncatulata)
Cercariae encyst on submerged/wet vegetation (metacercariae develop)
Ruminants ingest metacercariae
Metacercariae excyst in the duodenum, penetrate wall, enter peritoneum and invade Glissons capsule
Migration to the liver
Flukes reach sexual maturity (in ruminant bile duct)
Minimum period for life cycle completion is 17-19 weeks

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20
Q

What is the pathology of fasciola hepatica?

A

Parenchymal destruction during migration leading to inflammation and fibrosis
Rarely will damage large blood vessels leading to haemorrhage
Fluke in the bile duct can feed on animals blood leading to anaemia and cholestasis
Anaerobic environment can lead to Blacks disease (infectious necrotic hepatitis)

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21
Q

What are the acute clinical signs of fascoiola hepatica in sheep?

A 
Late autumn / early winter
Large numbers of migrating fluke in liver
Anaemia – Pale mucus membranes / weak
Hypoalbuminaemia
Rapidly fatal, animals often found dead
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22
Q

What are the clinical signs of sub-acute fascioloa hepatica in sheep?

A 
Late autumn / early winter
Rapid condition loss
Anaemia
Oedema (Submandibular “Bottle Jaw” or brisket oedema )
Colic
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23
Q

What are the clinical signs of chronic fascioloa hepatica in sheep?

A 
Winter / Early spring
Adult fluke sucking blood in bile ducts
Poor condition
Anaemia
Hypoalbuminaemia
Submandibular oedema
Chronic scour
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24
Q

How do goats present with fasciola hepatica?

A

Chronic form is most common although sub-acute is seen. Very rare to see sudden death.

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25
Q

What are the clinical signs of acute fascioloa hepatica in cattle?

A

Rare in cattle
Fibrous nature of liver
Acquired immunity does develop and provides protection (NB whilst antibody can be detected in sheep it appears to be non-protective)

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26
Q

What are the clinical signs of chronic fascioloa hepatica in cattle?

A

Similar presentation to sheep

Brisket and ventral oedema also seen

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27
Q

What are the clinical signs of subclinical fascioloa hepatica in cattle?

A

Increasingly recognised
Poor performance (reduced growth rate / reduced yield / loss of condition / predisposes to other disease)
Increased risk of Salmonella dublin?

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28
Q

How is faciola hepatica diagnosed?

A

Post mortem (fluke in parenchyma and bile duct)
Elevation of liver enzymes AST / GLDH (acute and chronic disease) / gGT (chronic disease bile duct damage)
Faecal egg count (adults must be present so only of use in chronic cases)
Eosinophilia – indicates parasitic infection (useful in subclinical cases)
Blood / bulk milk antibody ELISA (only indicates exposure)

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29
Q

What are the blood biochemistry changes in a faciola hepatica infection?

A 
Aspartate aminotransferase (AST) - Not liver specific, also produced from cardiac and skeletal muscle
Gamma glutamyltransferase (γGT) - Good indicator of bile duct damage
Glutamate dyhydrogenase (GLDH) - Liver specific, elevated in acute disease
Sorbitol dehydrogenase (SDH) - Liver specific, elevated in acute disease
Bilirubin - Conjugated increased with bile duct obstruction, unconjugated increased in haemolytic anaemia
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30
Q

What drugs can be used to treat liver fluke?

A 
Triclabendazole 
Nitroxynil 
Closantel 
Clorsulon 
Oxyclozanide 
Albendazole
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31
Q

Which drug can be used to treat immature fluke in sheep and cattle?

A

Triclabendazole

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32
Q

Which drug can be used to treat adult and late immature fluke in cattle?

A

Nitroxynil

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33
Q

Which drugs can be used to treat adult and late immature fluke in sheep?

A

Nitroxinil and closantel

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34
Q

Which drugs only treat adult fluke in cattle?

A

Clorsulon, oxyclozanide and albendazole

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35
Q

Which drugs only treat adult fluke in sheep?

A

Oxyclozanide and albendazole

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36
Q

How should acute fluke be treated?

A

Needs activity against early immature fluke (i.e. triclabendazole)

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37
Q

How is fluke treatment delivered?

A

Drench or subcutaneous injection

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38
Q

Which fluke products are licenced during lactation?

A

Oxyclozanide and albendazole

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39
Q

How can fluke infection be prevented?

A

Limit snail habitat
Prevent access to snail habitats (fence of marshy areas)
Application of molluscicides to pasture
Introduction of a predator e.g. geese
Prophylactic treatment (e.g. routine regular treatment of stock, treat when evidence of disease, treatment based on fluke forecast)

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40
Q

What other liver trematodes are there?

A

Fasciola gigantica
Fasciola magna
Dicrocoelium dendriticum

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41
Q

What is the aetiology of liver abscesses in large animals?

A

Bacteraemia from navel ill or another nidus of infection (e.g. ruminitis, FB)
Usually T. pyogenes or Fusobacterium necrophorum

42
Q

What happens if a liver abscess is found at slaughter?

A

Liver is discarded and the rest of the animal is eaten as normal

43
Q

What are the clinical signs of liver abscessation?

A 
Vague clinical signs, often subclinical 
Poor performance (poor yield, poor BCS, reduced growth rate)
44
Q

How can liver abscessation be prevented?

A

Limit subclinical ruminal acidosis

Add small quantities of roughage to the diet

45
Q

What complications may result from bacteraemia in large animals? (e.g. from a septic focus in the liver)

A

Peritonitis, endocarditis, caudal vena cava thrombosis syndrome

46
Q

What happens in caudal vena cava thrombosis syndrome?

A

Extension of infection into the caudal vena cava
Septic foci seed out in lungs establishing local abscesses
Erosion into major vessels can cause per-acute fatal haemorrhage
Animals usually found dead in a huge pool of blood

47
Q

What is the cause or ruminitis?

A

Chronic low rumen pH -> inflammation of the rumen mucosa

Common in barley beef animals fed 100% cereal diets +/- small quantities of forage

48
Q

What happens to the rumen mucosa in ruminitis?

A

Enlargement and hardening of the papillae
Excessive keratinization of the mucosa including food material and bacteria
Eventually rumen wall abscessation can occur which may extend into the liver

49
Q

What is the pathogenesis of Ragwort?

A

Contains pyrrolizidine alkaloids which are toxic to hepatocytes
The degree of liver damage depends on dose
Toxicity can be acute or chronic
It is often subclinical due to a large functional liver reserve

50
Q

What are the clinical signs of ragwort poisoning?

A

Dull, depressed, weight loss, poor doing, jaundice, subcutaneous oedema (due to hypoalbuminemia), colic, scour, photosensitization
Hepatic encephalopathy can occur - staggering, circling and blindness

51
Q

How is ragwort poisoning diagnosed?

A

History of exposure
Elevation of liver enzymes in serum
Histology of liver (biopsy or PM)
Post mortem changes (shrunken, fibrosed, slate-grey or mottled liver)

52
Q

How can ragwort poisoning be treated and prevented?

A

Symptomatic treatment

Prevent in other animals in the group

53
Q

Which species are most susceptible to copper toxicity?

A

Sheep

Esp certain breeds e.g. North Ronaldsay, Charollais, Texel and Suffolk breeds

54
Q

Why is copper toxicity becoming more common in cattle?

A

Over supplementation to avoid infertility

55
Q

What is the pathogenesis of copper toxicity?

A

Excess Cu is stored in the liver
Subclinical liver degeneration
Sudden mass release of Cu
Acute intravascular haemolysis -> prehepatic jaundice
Renal Cu excretion capacity overwhelmed -> nephromegaly and haemoglobinurea

56
Q

What are the clinical signs of acute copper poisoning?

A

Depression, colic, collapse, death

57
Q

What are the clinical signs of chronic copper poisoning?

A

Jaundice, anaemia, depression and anorexia, rumen stasis, colic, diarrhoea, recumbency and death
This is more common in cattle

58
Q

How is copper toxicity diagnosed?

A

Clinical signs
History of exposure to copper or over supplementation
Post mortem (widespread jaundice, hepatomegaly, distended bronze-black kidneys)
Plasma Cu >50mmol/L (Live animal)
Liver Cu >8,000 mmol/Kg (PM or biopsy?)
Kidney Cu >650 mmol/Kg (PM)

59
Q

How is copper toxicity treated?

A

None if haemolytic crisis has occurred
Remove from sources of Cu from diet
Ammonium tetrathiomolybdate described but not licensed in UK/EU
Fluids and supportive therapy

60
Q

How is copper toxicity prevented?

A

Only feed sheep concentrate designed for sheep (has low Cu)
Never graze sheep on pasture fertilised with pig manure
Calculate and monitor Cu intake

61
Q

Why may you do a liver biopsy in farm animals?

A

Liver copper estimations
Diagnosis of fatty liver
Histology in case of liver disease

62
Q

What are the dangers of liver biopsy?

A

Haemorrhage

Infection

63
Q

What are the landmarks for taking a liver biopsy in cattle?

A

Right had side, 11th rib space, ~20cm below transverse process

64
Q

What is the technique for taking a liver biopsy in cattle?

A 
Surgically prepare the site
Local anaesthetic in all layers 
1cm stab incision through the skin 
Introduce biopsy needle through the intercostal muscle towards the left elbow 
Biopsy using standard technique
65
Q

What are the predominant salmonella species in adult cattle?

A

S. Dublin, S. typhimurium

66
Q

What are the clinical signs of salmonella in adult cattle?

A

Diarrhoea, pyrexia, systemically ill, abortions, septicaemia, pneumonia polyarthritis, ear tip necrosis in calves

67
Q

What are the features of a salmonella carrier state?

A

Mixed infections common (often fasciola hepatica)
Source of infection is usually bought in cattle (or contaminated feed/pasture/water)
Can be an active or passive carrier
Shedding of the organism can be activated by stress

68
Q

How can salmonella be diagnosed in adult cattle?

A 
Is difficult as clinical signs and PM are not unique 
Enteritis – faecal samples 
Abortion – foetus, placenta 
Infected herd – slurry sample 
Screen for liver fluke
69
Q

How is salmonella treated in adult cattle?

A

Antibiotics e.g. amoxicillin and TMPS IM 5 days – prevent systemic disease but may increase length of carrier state and select for resistant strains (e.g. S. typhimurium DT104)
Culture and sensitivity is important

70
Q

What route should systemic antibiotics NOT be given to cattle?

A

Oral antibiotics will interfere with rumen flora in adult cattle but can be given to calves pre-weaning.

71
Q

What prevention and control measures can be used for salmonella in cattle?

A

Vaccination of non-clinical animals (dead vaccine, can also be used in face of an outbreak)
Closed herd
Disinfection protocols
Prevention of concurrent liver fluke infection
Wildlife biosecurity
Feed and pasture contamination
Clean water source (mains)

72
Q

What is winter dysentery?

A

A characteristic syndrome of diarrhoea and milk drop seen in groups of animals

73
Q

What are the clinical signs of winter dysentery?

A

Self limiting profuse dark diarrhoea, reduced milk yield (10-30%), colic

74
Q

What is the aetiology of winter dysentery?

A

Causal agent thought to be a corona virus with a tropism of GI and resp tracts

75
Q

What is the epidemiology of winter dysentery?

A

Very infectious, high morbidity, mortality is rare, short incubation period 3-7 days.

76
Q

How is winter dysentery diagnosed?

A

Clinical signs and history. Can look for virus in the faeces but this virus also found in normal animals
Important to differentiate from other causes e.g. salmonellosis

77
Q

How is winter dysentery treated?

A

Supportive, the disease is self limiting

78
Q

How can winter dysentery be prevented?

A

Standard biosecurity measures, infection is hard to control once established but will burn itself out in a couple of weeks

79
Q

What is the differential diagnosis for diarrhoea in adult cattle?

A 
Johnes disease 
Liver fluke 
GI parasites 
Coccidiosis 
BVD 
Babesiosis 
Malignant catarrhal fever 
Clostridial disease 
Endotoxaemia
80
Q

What are the causes of acute diarrhoea in adult cattle?

A 
Clinical ruminal acidosis 
Poisoning 
Endotoxaemia 
Ingestion/dietary 
Winter dysentery 
Malignant catarrhal fever 
Salmonellosis 
Abomasal ulcer 
BVD (transient infection)
81
Q

What are the causes of chronic diarrhoea in cattle?

A 
Johnes disease 
Micronutrient deficiency/toxicity 
Liver fluke 
Amyloidosis 
GI parasite
82
Q

Causes of diarrhoea in a group of cattle

A

Micronutrient deficiency/toxicity
GI parasites
BVD (acute/transient infection)
Winter dysentery

83
Q

Causes of diarrhoea in an individual cow

A 
Abomasal ulcer 
Endotoxaemia 
Malignant catarrhal fever 
Amyloidosis 
Johne’s disease 
BVD (mucosal disease in PI animal)
84
Q

Causes of diarrhoea in the individual cow or a group

A 
Poisoning 
Ruminal acidosis 
Ingestion/dietary 
Liver fluke 
Salmonellosis
85
Q

What questions would you ask in a case of diarrhoea?

A 
Individual or herd outbreak?
Acute/subacute/chronic?
Any animal movements or new animals onto farm?
Nutrition: any changes in feed?
Mortality/morbidity?
Milk drop?
Abortions?
86
Q

What can the diarrhoea look like in different conditions of the adult cow?

A 
Dark and foul smelling (occult blood)
Pale and pasty (rumen acidosis)
Watery (endotoxaemia)
Air bubbles (Johne’s)
Mucus, fibrinous casts (Salmonella)
Fresh blood
87
Q

Give a diagnostic plan for diarrhoea in adult cattle?

A 
History 
Clinical exam 
Faecal sample?
Blood?
PM?
Response to supportive treatment?
Consideration of zoonotic potential
88
Q

What is a treatment plan for diarrhoea in adult cattle?

A 
Supportive treatment (remove from current feed, transfaunation, introduce good quality hay) 
Absorbants such as kaolin 
Fluids 
NSAIDs 
Antibiotics?
Rumen supplements (no evidence)
89
Q

What factors play a role in whether salmonella infection leads to clinical disease?

A 
Serotype 
Concurrent infection 
Previous exposure 
Immune competence 
Colostrum 
Strain 
Viral load
90
Q

What is traumatic reticuloperitonitis (TRP)?

A

Aka. Hardware or tyre wire
Caused by fragments of metal being eaten by cattle and progressing to the reticulum where they may penetrate the rumenoreticular wall and migrate through the body.
Clinical signs vary

91
Q

What are the 4 main presentations of TRP?

A

Acute peritonitis
Chronic local peritonitis
Diffuse peritonitis
Sudden death

92
Q

How does acute peritonitis present?

A 
Anorexia 
Milk drop (>50% in 24hrs) 
Pyrexia 
Subacute abdominal pain, 'tucked-up' appearance
Reduced/absent rumination 
Firmer faeces 
Moderate abdominal fill and mild ruminal tympany 
Grunting 
Difficulty in rising and laying down 
Peculiar laying position e.g. lateral
93
Q

What are the differential diagnoses for an acute peritonitis presentation?

A

Traumatic reticulitis
Pericarditis
Pleuritis
Any painful abdominal condition

94
Q

How does chronic local peritonitis present?

A

Disappointing milk yield
Loss of body condition
Arched back, tense abdomen, smaller rumen, reduced rumen motility
Variable temperature (may be subnormal or slightly elevated)
Reduced faecal quantity with an increase in undigested particles
Mildly tachycardic
Vague signs of ill health, poor production and infertility

95
Q

What are the differential diagnoses for a chronic local peritonitis presentation?

A

Chronic indigestion
Ketosis
Pneumonia

96
Q

How does diffuse peritonitis present?

A 
Typically in recently calved animals 
Abdominal enlargement despite anorexia 
Absent or limited rumen movement 
Toxaemia and shock (skin tent time of the upper eyelid is more than 3 seconds) 
Dehydration 
Tachycardia (>120bpm) 
Scant faeces 
Pain on deep rectal palpation
97
Q

Why does sudden death occur in TRP?

A

Sudden death in apparently healthy cattle can result from migration of wire directly through the pericardial sac and perforation of either a coronary vessel or the heart itself

98
Q

How is TRP diagnosed?

A

History (sudden drop in milk over 24hr period)
Clinical exam (reduced rumen size, reduced rumen movement, reduced appetite, change in faecal constancy, reluctance to extend back on withers pinch, grunt on bar test, muffled heart sounds, distention of jugular veins, mild pyrexia)
Radiography
Ultrasonography
Exlap
Abdominal paracentesis – may show peritonitis
Blood tests (leucocytosis, neutrophilia with a left shift, acute phase proteins e.g. fibrinogen or haptoglobin)

99
Q

What are the 2 methods for rumenotomy?

A

Method 1 – create a temporary rumenostomy by suturing the edges of the rumen incision to the skin, this can be left as a semi-permanent stoma or closed at the end of surgery
Method 2 – using a Weingart frame, this is quicker and easier than rumenostomy

100
Q

What are some causes of chronic ruminal hypomobility syndrome?

A

Vagal indigestion
Botulism
Tetanus
Peritonitis

GI2 (27 decks)

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